Decreased CSF Concentrations of Homovanillic Acid and γ-Aminobutyric Acid in Alzheimer's Disease

Bareggi, Silvio R.; Franceschi, M.; Bonini, L.; Zecca, Luigi; Smirne, Salvatore

doi:10.1001/archneur.1982.00510230035010

Cited by 97 publications

(46 citation statements)

References 27 publications

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“…In fact, AD patients have been described as having high plasma cortisol concentrations in the morning [5] and an escape from dexamethasone suppression [19], Recently, we also found high plasma levels of (3-end in patients with Parkinson's disease (PD), even more elevated than those in our AD patients and reversed by substitutive therapy with /-dopa [II], Since it is known [10,14] that tuberoinfundibular dopaminergic activity (TIDA) has an inhibitory effect on pituitary |l-end release, we would like to interpret the similar findings in PD and AD patients as indicating a defi cit in TIDA. This agrees with the well-known dopamine deficit in PD and with several other biochemical data [1,7,12] indicating the same deficit in AD. On the other hand, if this hypothesis be true, one would also expect effects on PRL secretion, which we did not observe.…”

Section: Discussionsupporting

confidence: 92%

Neuroendocrinological Function in Alzheimer’s Disease

et al. 1988

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The neuroendocrine function is regulated by several neurotransmitters (acetylcholine, dopamine, somatostatin and noradrenaline) known to be reduced in brains of patients with Alzheimer’s disease (AD). Moreover, the hypothalamus also has pathological changes. In spite of these findings suggesting neuroendocrine dysfunctions, this function has seldom been investigated in AD patients so far. We have compared patients with clinically ‘probable’ AD of mild-to-moderate severity with nondemented age- and sex-matched controls. Plasma levels of prolactin (PRL), growth hormone (GH) and thyroid-stimulating hormone (TSH) were measured by commercially available radioimmunoassays (RIA) before and after stimulation with metoclopramide, /-dopa or thyrotropin-releasing hormone. Basal plasma levels of β-endorphin and β-lipotropin were measured by RIA after high-performance liquid chromatography. Basal and stimulated plasma levels of PRL, GH, TSH and β-lipotropin were similar in the two groups. Basal plasma levels of β-endorphin were significantly higher in the patient group. Of doubtful clinical importance, this might be attributed to decreased tuberoinfundibular dopaminergic activity and has also been seen in patients with Parkinson’s disease.

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Section: Discussionsupporting

confidence: 92%

Neuroendocrinological Function in Alzheimer’s Disease

et al. 1988

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“…In AD patients, there are reports of decreased 5-HT as well as decreased 5-HIAA in CSF [ 15,16] and in the brain [10][11][12]. To the best of our knowledge, a reduction in platelet 5-HT concentration in AD has not been reported before.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, the seroton ergic neurons in the raphe nuclei have been reported to be damaged by deposits of neurofibrillary tangles [5][6][7], More important, there are reports showing decreased lev els of serotonin (5-HT) and its metabolite 5-hydroxyin doleacetic acid (5-H1AA) in the brains of AD patients [8][9][10][11][12], However, there are conflicting reports on changes in cerebrospinal fluid (CSF) concentrations of 5-HT and 5-HIAA in AD. Some studies reported decreased levels of 5-HT and 5-HIAA in CSF in AD as compared to control subjects [12,14], whereas other studies did not find any significant differences [15,16].…”

Section: Introductionmentioning

confidence: 99%

Peripheral Serotonin in Alzheimer’s Disease

et al. 1995

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The platelet has been suggested to be a peripheral model of the central seroton-ergic neuron. This investigation was carried out in order to test the hypothesis that levels of serotonin (5-HT) in the platelet will be decreased in Alzheimer’s disease (AD) since neurochemical studies suggest that levels of 5-HT are decreased in the brain of AD patients. We investigated platelet and plasma 5-HT in a group of AD patients (n = 22) as well as in age-matched normal control subjects (n = 20). The results show that the platelet level of 5-HT was significantly reduced in AD (65.7 ± 28.41 ng/10⁸ platelets in AD vs. 112.9 ± 35.11 ng/10⁸ platelets in controls; p = 0.0001). There was no effect on the levels of its metabolite 5-hydroxyindoleacetic acid. These findings suggest that the peripheral serotonergic system in AD is adversely affected.

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“…There is evidence that GABAergic interneuron impairment might be involved in the pathogenesis of AD. These include reduced somatostatin immunoreactivity in the cerebral cortex from cases of AD [40] and a decrease in the cerebrospinal fluid concentrations of GABA in AD patients [41,42,43,44]. The loss of somatostatin immunoreactivity in AD brains is exacerbated by the presence of apolipoprotein (apo) E4, the major known genetic risk factor for AD [45].…”

Section: Discussionmentioning

confidence: 99%